This blog is about statistics, evolution, nutrition, lifestyle, and health issues. A combination of these issues. The focus is on quantitative research and how it can be applied in practice. But you may see other types of posts here (e.g., recipes, ideas, concepts, theories) from time to time.

Monday, February 28, 2011

Our body naturally produces as much as 10,000 IU of vitamin D based on a few minutes of sun exposure when the sun is high. Getting that much vitamin D from dietary sources is very difficult, even after “fortification”.

The above refers to pre-sunburn exposure. Sunburn is not associated with increased vitamin D production; it is associated with skin damage and cancer.

Solar ultraviolet (UV) radiation is generally divided into two main types: UVB (wavelength: 280–320 nm) and UVA (320–400 nm). Vitamin D is produced primarily based on UVB radiation. Nevertheless, UVA is much more abundant, amounting to about 90 percent of the sun’s UV radiation.

UVA seems to cause the most skin damage, although there is some debate on this. If this is correct, one would expect skin pigmentation to be our body’s defense primarily against UVA radiation, not UVB radiation. If so, one’s ability to produce vitamin D based on UVB should not go down significantly as one’s skin becomes darker.

Also, vitamin D and cholesterol seem to be closely linked. Some argue that one is produced based on the other; others that they have the same precursor substance(s). Whatever the case may be, if vitamin D and cholesterol are indeed closely linked, one would expect low cholesterol levels to be associated with low vitamin D production based on sunlight.

Bogh et al. (2010) recently published a very interesting study. The link to the study was provided by Ted Hutchinson in the comments sections of a previous post on vitamin D. (Thanks Ted!) The study was published in a refereed journal with a solid reputation, the Journal of Investigative Dermatology.

The study by Bogh et al. (2010) is particularly interesting because it investigates a few issues on which there is a lot of speculation. Among the issues investigated are the effects of total cholesterol and skin pigmentation on the production of vitamin D from UVB radiation.

The figure below depicts the relationship between total cholesterol and vitamin D production based on UVB radiation. Vitamin D production is referred to as “delta 25(OH)D”. The univariate correlation is a fairly high and significant 0.51.

25(OH)D is the abbreviation for calcidiol, a prehormone that is produced in the liver based on vitamin D3 (cholecalciferol), and then converted in the kidneys into calcitriol, which is usually abbreviated as 1,25-(OH)2D3. The latter is the active form of vitamin D.

The table below shows 9 columns; the most relevant ones are the last pair at the right. They are the delta 25(OH)D levels for individuals with dark and fair skin after exposure to the same amount of UVB radiation. The difference in vitamin D production between the two groups is statistically indistinguishable from zero.

So there you have it. According to this study, low total cholesterol seems to be associated with impaired ability to produce vitamin D from UVB radiation. And skin pigmentation appears to have little effect on the amount of vitamin D produced.

I hope that there will be more research in the future investigating this study’s claims, as the study has a few weaknesses. For example, if you take a look at the second pair of columns from the right on the table above, you’ll notice that the baseline 25(OH)D is lower for individuals with dark skin. The difference was just short of being significant at the 0.05 level.

What is the problem with that? Well, one of the findings of the study was that lower baseline 25(OH)D levels were significantly associated with higher delta 25(OH)D levels. Still, the baseline difference does not seem to be large enough to fully explain the lack of difference in delta 25(OH)D levels for individuals with dark and fair skin.

A widely cited dermatology researcher, Antony Young, published an invited commentary on this study in the same journal issue (Young, 2010). The commentary points out some weaknesses in the study, but is generally favorable. The weaknesses include the use of small sub-samples.

Monday, February 21, 2011

In this post on the China Study II data we have seen that wheat apparently displaces dietary fat a lot, primarily fat from animal sources. We have also seen in that post that wheat is strongly and positively associated with mortality in both the 35-69 and 70-79 age ranges, whereas dietary fat is strongly and negatively associated with mortality in those ranges.

This opens the door for the hypothesis that wheat increased mortality in the China Study II sample mainly by displacing dietary fat, and not necessarily by being a primary cause of health problems. In fact, given the strong displacement effect discussed in the previous post, I thought that this hypothesis was quite compelling. I was partly wrong, as you’ll see below.

A counterintuitive hypothesis no doubt, given that wheat is unlikely to have been part of the diet of our Paleolithic ancestors, and thus the modern human digestive tract may be maladapted to it. Moreover, wheat’s main protein (gluten) is implicated in celiac disease, and wheat contains plant toxins such as wheat germ agglutinin.

Still, we cannot completely ignore this hypothesis because: (a) the data points in its general direction; and (b) wheat-based foods are found in way more than trivial amounts in the diets of populations that have relatively high longevity, such as the French.

Testing the hypothesis essentially amounts to testing the significance of two mediating effects; of fat as a mediator of the effects of wheat on mortality, in both the 35-69 and 70-79 age ranges. There are two main approaches for doing this. One is the classic test discussed by Baron & Kenny (1986). The other is the modern test discussed by Preacher & Hayes (2004), and extended by Hayes & Preacher (2010) for nonlinear relationships.

I tested the meditating effects using both approaches, including the nonlinear variation. I used the software WarpPLS for this; the results below are from WarpPLS outputs. Other analyses of the China Study data using WarpPLS can be found here (calorie restriction and longevity), and here (wheat, rice, and cardiovascular disease). For yet other studies, click here.

The graphs below show the path coefficients and chance probabilities of two models. The one at the top-left suggests that wheat flour consumption seems to be associated with a statistically significant increase in mortality in the 70-79 age range (beta=0.23; P=0.04). The effect in the 35-69 age range is almost statistically significant (beta=0.22; P=0.09); the likelihood that it is due to chance is 9 percent (this is the meaning of the P=0.09=9/100=9%).

The graph at the bottom-right suggests that the variable “FatCal”, which is the percentage of calories coming from dietary fat, is indeed a significant mediator of the relationships above between wheat and mortality, in both ranges. But “FatCal” is only a partial mediator.

The reason why “FatCal” is not a “perfect” mediator is that the direct effects of wheat on mortality in both ranges are still relatively strong after “FatCal” is added to the model (i.e., controlled for). In fact, the effects of wheat on mortality don’t change that much with the introduction of the variable “FatCal”.

This analysis suggests that, in the China Study II sample, one of wheat’s main sins might indeed have been to displace dietary fat from animal sources. Wheat consumption is strongly and negatively associated with dietary fat (beta=-0.37; P<0.01), and dietary fat is relatively strongly and negatively associated with mortality in both ranges (more in the 70-79 age range).

Why is dietary fat more protective in the 70-79 than in the 35-69 age range, with the latter effect only being significant at the P=0.10 level (a 10 percent chance probability)? My interpretation is that, as with almost any dietary habit, it takes years for a chronically low fat diet to lead to problems. See graph below; fat was not a huge contributor to the total calorie intake in this sample.

The analysis suggests that wheat also caused problems via other paths. What are them? We can’t say for sure based on this dataset. Perhaps the paths involve lectins and/or gluten. One way or another, the relationship is complex. As you can see from the graph below, the relationship between wheat consumption and mortality is nonlinear for the 70-79 age range, most likely due to confounding factors. The effect size is small for the 35-69 age range, even though it looks linear or quasi-linear in that range.

As you might recall from this post, rice does NOT displace dietary fat, and it seems to be associated with increased longevity. Carbohydrate content per se does not appear to be the problem here. Both rice and wheat foods are rich in them, and have a high glycemic index. Wheat products tend to have a higher glycemic load though.

And why is dietary fat so important as to be significantly associated with increased longevity? This is not a trivial question, because if too much of that fat is stored as body fat it will actually decrease longevity. Dietary fat is very calorie-dense, and can be easily stored as body fat.

Dietary fat is important for various reasons, and probably some that we don’t know about yet. It leads to the formation of body fat, which is not only found in adipocytes or used only as a store of energy. Fat is a key component of a number of important tissues, including 60 percent of our brain. Since fat in the human body undergoes constant turnover, more in some areas than others, lack of dietary fat may compromise the proper functioning of various organs.

Without dietary fat, the very important fat-soluble vitamins (A, D, E and K) cannot be properly absorbed. Taking these vitamins in supplemental form will not work if you don’t consume fat as well. A very low fat diet is almost by definition a diet deficient in fat-soluble vitamins, even if those vitamins are consumed in large amounts via supplements.

Moreover, animals store fat-soluble vitamins in their body fat (as well as in organs), so we get these vitamins in one of their most natural and potent forms when we consume animal fat. Consuming copious amounts of olive and/or coconut oil will not have just the same effect.

Sunday, February 13, 2011

The idea that protein leaches calcium from the bones has been around for a while. It is related to the notion that protein, especially from animal foods, increases blood acidity. The body then uses its main reservoir of calcium, the bones, to reduce blood acidity. Chris Masterjohn does not agree with this idea. This post generally supports Chris’s view, and adds a twist to it, related to plant protein consumption.

The “eat-meat-lose-bone” idea has apparently become popular due to the position taken by Loren Cordain on the topic. Dr. Cordain has also made several important and invaluable contributions to our understanding of the diets of our Paleolithic ancestors. He has argued in his book, The Paleo Diet, and elsewhere (see, e.g., here) that to counter the acid load of protein one should eat fruits and vegetables. The latter are believed to have an alkaline load.

If the idea that protein leaches calcium from the bones is correct, one would expect to see a negative association between protein consumption and bone mineral density (BMD). This negative association should be particularly strong in people aged 50 and older, who are more vulnerable to BMD losses.

As it turns out, this idea appears to be correct only for plant protein. Animal protein seems to be associated with an increase in BMD, at least according to a study by Promislow et al. (2002). The study shows that there is a positive multivariate association between animal protein consumption and BMD; an association that becomes negative when plant protein consumption is considered.

The study focused on 572 women and 388 men aged 55–92 years living in Rancho Bernardo, California. Food frequency questionnaires were administered in the 1988–1992 period, and BMD was measured 4 years later. The bar chart below shows the approximate increases in BMD (in g/cm^2) for each 15 g/d increment in protein intake.

The authors reported increments in BMD for different increments of protein (15 and 5 g/d), so the results above are adjusted somewhat from the original values reported in the article. Keeping that in mind, the increment in BMD for men due to animal protein was not statistically significant (P=0.20). That is the smallest bar on the left.

Does protein leach calcium from the bones? Based on this study, the reasonable answers to this question are yes for plant protein, and no for animal protein. For animal protein, it seems to be quite the opposite.

Even more interesting, calcium intake did not seem to be much of a factor. BMD gains due to animal protein seemed to converge to similar values whether calcium intake was high, medium or low. The convergence occurred as animal protein intake increased, and the point of convergence was between 85-90 g/d of animal protein intake.

And high calcium intakes did not seem to protect those whose plant protein consumption was high.

The authors do not discuss specific foods, but one can guess the main plant protein that those folks likely consumed. It was likely gluten from wheat products.

Are the associations above due to: (a) the folks eating animal protein consuming more fruits and vegetables than the folks eating plant protein; or (b) something inherent to animal foods that stimulates an increase in the absorption of dietary calcium, even in small amounts?

This question cannot be answered based on this study; it should have controlled for fruit and vegetable consumption for that.

Sunday, February 6, 2011

Spending too much time sitting down is clearly unnatural, particularly if you sit down on very comfortable chairs. Sitting down per se is probably natural, given the human anatomy, but not sitting down for hours in the same position. Also, comfortable furniture is an apparently benign Neolithic invention, but over several years it may stealthily contributed to the metabolic syndrome and the diseases of civilization.

Getting an elevated workstation may be a bit expensive. At work, you may have to go through a bit of a battle with your employer to get it (unless you are "teh boz"), only to find out that having to work standing up all the time is not what you really wanted. That may not be very natural either. So what is one to do? One possible solution is to buy a small foldable plastic table (or chair) like the one on the figure below, which may cost you less than $10, and put it on your work desk. I have been doing this for quite a while now, and it works fine for me.

The photo above shows a laptop computer. Nevertheless, you can use this table-over-table approach with a desktop computer as well. And you still keep the space under the foldable table, which you can use to place other items. With a desktop computer this approach would probably require two foldable tables to elevate the screen, keyboard, and mouse. This approach also works for reading documents and writing with a pen or pencil; just put a thick sheet of paper on the foldable table to make a flat surface (if the foldable table’s surface is not flat already). And you don’t have to be standing up all the time; you can sit down as well after removing the foldable table. It takes me about 5 seconds to do or undo this setup.

When you sit down, you may want to consider using a pillow like the one on the photo to force yourself to sit upright. (You can use it as shown, or place the pillow flat on the chair and sit on its edge.) Sitting on a very comfy chair with back support prevents you from using the various abdominal and back muscles needed to maintain posture. As a result, you may find yourself unusually prone to low back injuries and suffering from “mysterious” abdominal discomfort. You will also very likely decrease your nonexercise activity thermogenesis (NEAT), which is a major calorie expenditure regulator.

With posture stabilization muscles, as with almost everything else in the human body, the reality is this: if you don’t use them, you lose them.

Ned Kock

About Me

I strongly believe that lifestyle, nutrition and exercise habits that are compatible with our evolutionary past are the key to optimal health. On the other hand, I do not believe that closely mimicking life in the Paleolithic is optimal for health, or even viable. I am a researcher, software developer, consultant, and college professor. Two of my main areas of research are nonlinear variance-based structural equation modeling, and evolutionary biology as it applies to the study of human-technology interaction. My degrees are in engineering (B.E.E.), computer science (M.S.), and business (Ph.D.). I am interested in the application of science, statistics, and technology to the understanding of human health and behavior. I blog about evolution, health, statistics, and technology. My personal web site contains links to my contact information and freely available articles related to the topics of my blogs: nedkock.com.

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